期刊文献+

软骨细胞损伤及其自噬与关节炎 被引量:3

Chondrocyte injury and autophagy and arthritis
原文传递
导出
摘要 骨关节炎等疾病的致病因素主要在软骨细胞上,软骨细胞退变造成骨软骨关节受损,加上炎症细胞浸润,导致关节类疾病很难治愈。软骨细胞除去受损死亡外,自噬也是使其数量减少的一个主要原因,自噬其实在某种意义上对机体细胞是一种有利性功能,这其中就包括软骨细胞,细胞通过自我消化即分解胞内大分子物质来获取能量以维持细胞正常生代谢。软骨细胞的自噬通常在氧气含量过低的环境中进行,依据关节内的细小变化作调整细胞代谢,从而维持关节软骨生物学功能,研究发现Beclin1基因在自噬体系中起控制作用。对自噬在软骨细胞中的作用性对骨关节炎的影响进行分析,如果能降低软骨细胞的死亡率,可以有效地减缓甚至逆转上述疾病的发病,而行之有效的治疗该类疾病的好方法是通过研究软骨细胞的自噬,进而把控软骨的病变进程,减缓甚至是骨关节炎类疾病的病变及恶化。 The cause of diseases such as osteoarthritis,mainly on the cartilage chondrocytes back altered osteogenesis articular cartilage damage,and inflammatory cells infiltration,lead to joint diseases hard to cure.To remove damaged cartilage cell death,autophagy is the decrease in the number of make it one of the main reasons that autophagy is in some sense is good for the body’s cells is a kind of sexual function,including the cartilage cells,cell self digestion by decomposition intracellular macromolecular material to obtain energy to maintain normal cell metabolism.The autophagy of chondrocytes is usually carried out in an environment with low oxygen content,so as to adjust the cell metabolism according to the small changes in the joint,so as to maintain the biological function of articular cartilage.The study found that Beclin1 gene plays a role in the autophagy system,and this study analyzes the effects of autophagy on osteoarthritis in chondrocytes.Objective: If we can reduce the mortality of cartilage cells,can effectively slow down or even reverse the onset of the disease,and a good way to effective treatment of the disease is through the study of autophagy,cartilage cells,in turn,the accused of cartilage lesions in the process,slow and even bone arthritis diseases lesions and deterioration.
作者 王红光 WANG Hong-guang(Department of orthopedics Jiamusi Central Hospital, Jiamusi 154000, China)
出处 《微量元素与健康研究》 CAS 2019年第2期57-59,共3页 Studies of Trace Elements and Health
关键词 软骨 软骨细胞 自噬 损伤 关节炎 cartilage chondrocytes autophagy injury arthritis
  • 相关文献

参考文献3

二级参考文献95

  • 1佟晓杰,张彩顺,曹德寿,刘承吉,于频.脱细胞异体神经移植物桥接大鼠坐骨神经缺损促进神经肌结构重建和功能恢复的实验研究[J].解剖学报,2005,36(1):1-5. 被引量:9
  • 2Carams B, Taniguchi N, Otsuki S, et al.Autophagy is a protective mechanism in normal cartilage, and its aging-related loss is linked with cell death and osteoarthritis[J].Arthritis & Rheumatism, 2010, 62 ( 3 ) : 791-801.
  • 3Tasdemir E, Maiuri M C, Galluzzi L, et al.Regulation of autophagy by cytoplasmic p53[J].Nat Cell Biol, 2008, 10 ( 6 ) : 676-687.
  • 4Abramson S B, Attur M.Developments in the scientific understanding of osteoarthritis[J].Arthritis Res Ther, 2009, 11 ( 3 ) : 227.
  • 5Gobbi A, Kon E, Berruto M, et al.Patellofemoral full-thickness chondral defects treated with hyalograft-C: a clinical, arthroscopic, and histologie review[J].Am J Sports Med, 2006, 34 ( 11 ) : 1763- 1773.
  • 6Heraud F, Heraud A, Harmand M F.Apoptosis in normal and osteoarthritic human articular cartilage[J].Ann Rheum Dis, 2000, 59 ( 12 ) : 959-965.
  • 7Kim J, Xu M, Xo R, et al.Mitochondrial DNA damage is involved in apoptosis caused by pro-inflammatory cytokines in human OA ehondrocytes[J].Osteoarthritis and Cartilage, 2010, 18 ( 3 ) : 424- 432.
  • 8Follis A V, Chipuk J E, Fisher J C, et al.PUMA binding induces partial unfolding within BCL-xL to disrupt p53 binding and promote apoptosis[J].Nat Chem Biol, 2013, 9 ( 3 ) : 163-168.
  • 9Montero J, Dutta C, van Bodegom D, et al.p53 regulates a non- apoptotic death induced by ROS[J].Cell Death Differ, 2013, 20 ( 11 ): 1465 - 1474.
  • 10Lundgreen K, Lian 0, Scott A, et al.Increased levels of apoptosis and p53 in partial-thickness supraspinatus tendon tears[J].Knee Surgery, Sports Traumatology, Arthroscopy, 2013, 21 ( 7 ) : 1636-1641.

共引文献42

同被引文献35

引证文献3

二级引证文献20

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部